TY - JOUR
T1 - Transcriptomic analyses of primary astrocytes under TNFα treatment
AU - Birck, Cindy
AU - Koncina, Eric
AU - Heurtaux, Tony
AU - Glaab, Enrico
AU - Michelucci, Alessandro
AU - Heuschling, Paul
AU - Grandbarbe, Luc
N1 - Funding Information:
This work was supported by the University of Luxembourg . Cindy Birck is thankful to the doctoral school in systems and molecular biomedicine of the University of Luxembourg for providing a bench fee grant to realize microarrays analyses. Enrico Glaab acknowledges support by grants from the Fonds Nationale de la Recherche Luxembourg ( C13/BM/5782168 and NCER-PD I1R-BIC-PFN-15NCER ).
Publisher Copyright:
© 2015 The Authors.
PY - 2016/3/1
Y1 - 2016/3/1
N2 - Astrocytes, the most abundant glial cell population in the central nervous system, have important functional roles in the brain as blood brain barrier maintenance, synaptic transmission or intercellular communications [1,2]. Numerous studies suggested that astrocytes exhibit a functional and morphological high degree of plasticity. For example, following any brain injury, astrocytes become reactive and hypertrophic. This phenomenon, also called reactive gliosis, is characterized by a set of progressive gene expression and cellular changes [3]. Interestingly, in this context, astrocytes can re-acquire neurogenic properties. It has been shown that astrocytes can undergo dedifferentiation upon injury and inflammation, and may re-acquire the potentiality of neural progenitors [4,5,6,7].To assess the effect of inflammation on astrocytes, primary mouse astrocytes were treated with tumor necrosis factor α (TNFα), one of the main pro-inflammatory cytokines. The strength of this study is that pure primary astrocytes were used. As microglia are highly reactive immune cells, we used a magnetic cell sorting separation (MACS) method to further obtain highly pure astrocyte cultures devoid of microglia.Here, we provide details of the microarray data, which have been deposited in the Gene Expression Omnibus (GEO) under the series accession number GSE73022. The analysis and interpretation of these data are included in Gabel et al. (2015). Analysis of gene expression indicated that the NFκB pathway-associated genes were induced after a TNFα treatment. We have shown that primary astrocytes devoid of microglia can respond to a TNFα treatment with the re-expression of genes implicated in the glial cell development.
AB - Astrocytes, the most abundant glial cell population in the central nervous system, have important functional roles in the brain as blood brain barrier maintenance, synaptic transmission or intercellular communications [1,2]. Numerous studies suggested that astrocytes exhibit a functional and morphological high degree of plasticity. For example, following any brain injury, astrocytes become reactive and hypertrophic. This phenomenon, also called reactive gliosis, is characterized by a set of progressive gene expression and cellular changes [3]. Interestingly, in this context, astrocytes can re-acquire neurogenic properties. It has been shown that astrocytes can undergo dedifferentiation upon injury and inflammation, and may re-acquire the potentiality of neural progenitors [4,5,6,7].To assess the effect of inflammation on astrocytes, primary mouse astrocytes were treated with tumor necrosis factor α (TNFα), one of the main pro-inflammatory cytokines. The strength of this study is that pure primary astrocytes were used. As microglia are highly reactive immune cells, we used a magnetic cell sorting separation (MACS) method to further obtain highly pure astrocyte cultures devoid of microglia.Here, we provide details of the microarray data, which have been deposited in the Gene Expression Omnibus (GEO) under the series accession number GSE73022. The analysis and interpretation of these data are included in Gabel et al. (2015). Analysis of gene expression indicated that the NFκB pathway-associated genes were induced after a TNFα treatment. We have shown that primary astrocytes devoid of microglia can respond to a TNFα treatment with the re-expression of genes implicated in the glial cell development.
KW - Gene expression
KW - Inflammation
KW - Microarrays
KW - Primary astrocytes
UR - http://www.scopus.com/inward/record.url?scp=84947815245&partnerID=8YFLogxK
UR - https://www.ncbi.nlm.nih.gov/pubmed/26981349
U2 - 10.1016/j.gdata.2015.11.005
DO - 10.1016/j.gdata.2015.11.005
M3 - Article
C2 - 26981349
AN - SCOPUS:84947815245
SN - 2213-5960
VL - 7
SP - 7
EP - 11
JO - Genomics Data
JF - Genomics Data
ER -